We are studying the role of DNA repair processes in cancer and senescence. The goal is to determine whether there are detectable deficiencies in DNA repair in these two related conditions. Gene specific DNA repair has been measured in cells from patients with cancer prone and premature aging syndromes. Whereas we can not detect changes or deficiencies in the cancer prone syndromes, there is a lack of preferential DNA repair of active genes in at least one premature aging syndrome, Cockayne syndrome. In the human syndrome, Fanconi's anemia, we find that there is a deficiency in DNA repair, for both DNA lesions introduced by cisplatin. We have investigated the role of DNA repair in drug resistance. In cisplatin resistant human ovarian cancer cell lines we found a gene specific DNA repair alteration: an increase in the DNA repair efficiency of cisplatin interstrand crosslinks. This may be an important element in the resistant phenotype. Telomeric length is one of the best available biomarkers of aging. A shortening of telomeric length with aging has been observed in many biological systems. We are measuring DNA damage and repair in these critical end-regions of the chromosomes that are also very important for genomic stability.